Ask about this productRelated genes to: NR2C2 Blocking Peptide
- Gene:
- NR2C2 NIH gene
- Name:
- nuclear receptor subfamily 2 group C member 2
- Previous symbol:
- TR4
- Synonyms:
- TAK1, TR2R1, hTAK1
- Chromosome:
- 3p25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-15
- Date modifiied:
- 2016-10-05
Related products to: NR2C2 Blocking Peptide
Related articles to: NR2C2 Blocking Peptide
- Aging increases the risk and worsens the prognosis of traumatic brain injury. Neutrophils contribute to the secondary neuroinflammatory response after TBI. Nevertheless, the biological functions and underlying mechanisms contributing to the age-related heterogeneity of neutrophils in elderly individuals with TBI remain inadequately understood. The study identified a unique neutrophil subpopulation with elevated IL-10 expression, functionally enriched in young TBI tissues. CellChat analysis revealed significant intercellular communication between IL-10neutrophils and endothelial cells, with elevated expression of Vegfa. GO/KEGG analysis exhibit characteristics associated with reducing inflammatory responses, inhibiting oxidative stress, promoting angiogenesis and tissue remodeling. The IL-10 Ab intervention led to a deterioration in neurological outcomes in young TBI. SCENIC analysis demonstrated that the transcription factor NR2C2 regulates the distinct neutrophils. Transplantation experiments using GFP mouse bone marrow indicated that it could be a source of skull bone marrow. Transcriptome sequencing confirmed that phenotypic changes in dHL-60 cells, following NR2C2 overexpression, activate signaling pathways involved in Complement and coagulation cascades Immune, Hematopoietic cell lineage Immune, Jak STAT and Toll like receptor. The regulation of NR2C2 was achieved through siRNA knockdown technology to mitigate the effects of NO-prednisolone. NR2C2 overexpression, induced by NO-prednisolone, leads to the production of IL-10VEGF-αneutrophils in the brain tissue of aged mice with TBI, resulting in improved blood-brain barrier integrity, reduced pathological changes in brain tissue injury, inhibition of neuroinflammation, and significant enhancement of neurobehavioral function. CONCLUSION: This study explored the role of a specific subset of skull-derived IL-10VEGF-αneutrophils in TBI, with an emphasis on age-related immune cell heterogeneity. The findings indicate that these neutrophils exhibit anti-inflammatory and reparative properties, and are associated with the transcription factor NR2C2 and the potential therapeutic agent NO-prednisolone. This research provides potential interventions for treating TBI in the aging population. - Source: PubMed
Publication date: 2026/05/18
Cheng ShiyiQu JiahuaZhu YongqiZhu JueLu ZhichaoShi WeiWang ChenxingWang Wei - Growth traits in pigs are governed by complex polygenic architectures, with most associated loci residing in non-coding regions that exert substantial influence on economically relevant phenotypes. However, the molecular mechanisms underlying these regulatory elements remain poorly characterized. In this study, a non-coding mutation-designated as NR2C2 recognition motif sequence variation (NRMSV), located 2083 bp upstream of the HMGA1 gene-was identified as a functional modulator of growth traits in a three-generation Eurasian hybrid pig population. NR2C2 is a nuclear receptor implicated in skeletal development and metabolic regulation, while HMGA1 is a key determinant of body size across mammalian species. In embryonic fibroblasts, where NR2C2 is abundantly expressed, the mutant NRMSV suppressed transcriptional activity, functioning as a silencer. In contrast, in bone marrow mesenchymal stem cells, characterized by low NR2C2 expression, the same allele acted as a robust transcriptional enhancer. Knockdown of NR2C2 in embryonic fibroblasts abrogated this repression and restored enhancer activity, confirming the context-dependent, bidirectional regulatory effect of NRMSV on HMGA1 expression. These findings establish the NR2C2-NRMSV-HMGA1 pathway as a novel regulatory mechanism underpinning phenotypic variation in pig growth traits, offering mechanistic insights into mammalian developmental regulation and informing targeted genomic selection for improved productivity in porcine breeding programs. - Source: PubMed
Xie Li-ShiZhang Shu-RunMu Chang-GaiYuan MingWang ManGao Xuan-YuShi XianGao YunDeng Jia-KunYin Ting-TingWu Ru-NianWang Li-GangLi Jian-BoZhang Ya-Ping - Despite advancements in therapeutic strategies, metastatic prostate cancer (mPCa) remains challenging to treat, with limited clinical efficacy and poor prognosis. Anoikis resistance in tumor cells is crucial for their survival in the vascular system and plays a key role in metastasis. Therefore, investigating the molecular mechanisms of metastasis and anoikis resistance is essential for identifying novel therapeutic targets and strategies. In this study, we found that YEATS domain-containing 2 (YEATS2) plays a critical role in promoting PCa metastasis by suppressing anoikis. We observed that YEATS2 expression was elevated in mPCa and associated with poor clinical outcomes. Knockdown of YEATS2 reduced the metastatic potential of PCa cells both in vivo and in vitro, whereas its overexpression inhibited anoikis and promoted metastasis by upregulating the expression of the DNA damage repair gene RAD50. Mechanistically, YEATS2 increases chromatin accessibility at the RAD50 promoter region by recognizing H3K27ac and subsequently recruits the transcription factor NR2C2. Mirin suppressed lymph node metastasis of PCa cells in vivo. Our study demonstrated a novel function of the YEATS2/NR2C2/RAD50 axis in regulating DNA damage responses and anoikis resistance in PCa metastasis, highlighting an important pathway that drives metastatic progression and offering potential new strategies for treating mPCa. - Source: PubMed
Publication date: 2026/02/18
Li HaoranSong YarongCong YukunWang ChuxiongChen KangLiu ChunyuZhou MenghaoJu YunjieChen JinyuChen LiangXing Yifei - N-terminal acetyltransferases are emerging as potential therapeutic targets in cancer. N-alpha-acetyltransferase 30 (NAA30), which serves as the catalytic subunit of the NATC complex. However, the role of NAA30 in ovarian cancer remains unknown. In this study, we found that NAA30 expression was abnormally upregulated in ovarian cancer tissues compared to normal tissues. Functionally, NAA30 promoted cell proliferation, migration, and invasion in ovarian cancer cells. Moreover, in vivo experiments revealed that NAA30 enhanced tumor growth and intraperitoneal metastasis in mouse models. We further explored the regulatory mechanisms underlying NAA30 upregulation. Dual-luciferase assays demonstrated that the transcription factor nuclear receptor subfamily 2 group C member 2 (NR2C2) significantly enhanced the transcriptional activity of the NAA30 promoter. Besides, NR2C2 increased the migratory, invasive, and proliferative capabilities of ovarian cancer cells. Importantly, NAA30 knockdown reversed the pro-tumorigenic effects of NR2C2 overexpression on the malignant phenotype. To identify the downstream targets of NAA30, we employed IP-LC/MS and N-terminal acetylation modification omics. Actin-Related Protein 2/3 Complex Subunit 1B (ARPC1B) was identified as a direct target of NAA30. It was demonstrated that NAA30 protein binds to ARPC1B protein and that NAA30 knockdown enhanced the polyubiquitination of ARPC1B and promotes its degradation. Crucially, the re-expression of ARPC1B in NAA30-silenced cells effectively restored these malignant phenotypes. These findings highlight the critical role of the NR2C2-NAA30-ARPC1B axis in ovarian cancer progression and provide more foundation for the development of more effective treatment strategies for patients with ovarian cancer. - Source: PubMed
Xu LiwenZheng FeiWang DandanYang Qing - Vitamin D deficiency is associated with the risk of atopic diseases and respiratory infections. The activated vitamin D receptor (VDR) forms a dimer with the retinoid X receptor alpha (RXRA) and binds to VDR/RXRA composite elements (CEs) in enhancers of target genes. However, VDR/RXRA CEs are identified in only 11.5% of cases in ChIP-Seq peaks. Our hypothesis was that VDR could form a VDR-Partner complex with transcription factor for which CEs have not yet been identified. We utilized Web-MCOT to search for novel VDR/Partner CEs in regulatory DNA. The potential formation of the VDR-Partner protein complex was assessed using the AlphaFold machine learning model. Through real-time RT-PCR, we measured the expression of immune system genes in a culture of U937 macrophage-like cells incubated with the active metabolite of vitamin D, calcitriol. We have predicted novel VDR/NR2C2 and VDR/PPARG CEs in the regulatory regions of immune system genes. We found potential synergism of VDR/NR2C2 and VDR/RXRA CEs in relation to the gene, as well as potential synergism of VDR/PPARG and VDR/RXRA CEs for . Predicting new regulatory relationships through the identification of new potential VDR/Partner CEs may provide insight into the deep mechanisms of vitamin D involvement in the pathogenesis of atopic dermatitis, bronchial asthma, allergic rhinitis, and pulmonary infections. - Source: PubMed
Publication date: 2025/12/30
Popov Alexey VOshchepkov Dmitry YuKononchuk Vladislav VKalinina Tatiana SValembakhov Ilya SLukin Alexander DKondyurina Elena GZelenskaya Vera VVavilin Valentin